Hodgkin lymphoma in the Swiss HIV Cohort Study

International Agency for Research on Cancer, Lyon, France.
Blood (Impact Factor: 10.45). 03/2009; 113(23):5737-42. DOI: 10.1182/blood-2009-02-204172
Source: PubMed


Hodgkin lymphoma (HL) risk is elevated among persons infected with HIV (PHIV) and has been suggested to have increased in the era of combined antiretroviral therapy (cART). Among 14,606 PHIV followed more than 20 years in the Swiss HIV Cohort Study (SHCS), determinants of HL were investigated using 2 different approaches, namely, a cohort and nested case-control study, estimating hazard ratios (HRs) and matched odds ratios, respectively. Forty-seven incident HL cases occurred during 84,611 person-years of SHCS follow-up. HL risk was significantly higher among men having sex with men (HR vs intravenous drug users = 2.44, 95% confidence interval [CI], 1.13-5.24) but did not vary by calendar period (HR for 2002-2007 vs 1995 or earlier = 0.65, 95% CI, 0.29-1.44) or cART use (HR vs nonusers = 1.02, 95% CI, 0.53-1.94). HL risk tended to increase with declining CD4(+) cell counts, but these differences were not significant. A lower CD4(+)/CD8(+) ratio at SHCS enrollment or 1 to 2 years before HL diagnosis, however, was significantly associated with increased HL risk. In conclusion, HL risk does not appear to be increasing in recent years or among PHIV using cART in Switzerland, and there was no evidence that HL risk should be increased in the setting of improved immunity.

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    • "Table 1 Cohort study design features of cancer risk in HIV/AIDS patients. Study, year (reference) Country Study type Period of follow-up Number of patients Total number of person- years Number of cancers Dorrucci et al., 2001 [27] Italy Cohort 1981—1998 483 3364 6 Bower et al., 2003 [29] UK RL a 1986—2001 8400 22,694 11 Bower et al., 2004 [30] UK Cohort 1984—2003 8640 40,126 26 Hessol et al., 2004 [31] USA RL a 1994—2001 1554 7909 41 Biggar et al., 2006 [15] USA RL a 1980—2002 317,428 477,368 173 D'Souza et al., 2008 [32] USA Cohort 1984—2006 6972 100,000 69 Franceschi et al., 2008 [33] Switzerland Cohort 1984—2006 12,959 73,412 597 Polesel et al., 2008 [34] Switzerland Cohort 1984—2006 12,959 75,222 429 Engels et al., 2008 [35] USA Cohort 1991—2002 57,350 186,157 871 Crum-Cianflone et al., 2009 [4] USA Cohort 1984—2006 4498 33,486 446 Clifford et al., 2009 [36] Switzerland Cohort 1984—2007 14,606 84,611 47 Dal Maso et al., 2009 [43] Italy RL a 1986—2004 21,951 101,668 1995 Leewen et al., 2009 [20] Australia Cohort 1982—2004 37,407 311,496 2283 Powles et al., 2009 [41] UK Cohort 1983—2007 11,112 71,687 156 Buchacz et al., 2010 [37] USA Cohort 1994—2007 8070 3000 16 Crum-Cianflone, 2010 [39] USA Cohort 1985—2008 4506 37,806 66 Franceschi et al., 2010 [42] Switzerland RL a 1985—2006 9429 53,715 1460 Seaberg et al., 2010 [40] USA Cohort 1984—2007 6972 77,320 933 Besson et al., 2011 [38] France RL a 1993—1998 80,000 230,173 900 Kirk et al., 2001 [24] Europe Cohort 1994—2000 8471 26,764 222 Franzetti et al., 2012 [10] "
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    ABSTRACT: After highly active antiretroviral therapy (HAART) became widespread, several studies demonstrated changes in the incidence of defining and non-defining AIDS cancers among HIV/AIDS patients. We conducted a systematic review of observational studies evaluating the incidence of malignancies before and after the introduction of HAART in people with HIV/AIDS. Eligible studies were searched up to December 2012 in the following databases: Pubmed, Embase, Scielo, Cancerlit and Google Scholar. In this study, we determined the cancer risk ratio by comparing the pre- and post-HAART eras. Twenty-one relevant articles were found, involving more than 600,000 people with HIV/AIDS and 10,891 new cases of cancers. The risk for the development of an AIDS-defining cancer decreased after the introduction of HAART: Kaposi's sarcoma (RR = 0.30, 95% CI: 0.28–0.33) and non-Hodgkin's lymphoma (RR = 0.52, 95% CI: 0.48–0.56), in contrast to invasive cervical cancer (RR = 1.46, 95% CI: 1.09–1.94). Among the non-AIDS-defining cancers, the overall risk increased after the introduction of HAART (RR = 2.00, 95% CI: 1.79–2.23). The incidence of AIDS-defining cancers decreased and the incidence of non-AIDS-defining cancers increased after the early use of HAART, probably due to better control of viral replication, increased immunity and increased survival provided by new drugs.
    Journal of Infection and Public Health 10/2014; 8(1). DOI:10.1016/j.jiph.2014.08.003
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    • "The incidence of Hodgkin lymphoma has not fallen in HIV infected patients in the era of HAART [3]–[5]. One of the main challenges for clinicians is to rapidly make a diagnosis of Hodgkin lymphoma among patients with non-specific symptoms such as fever, sweats and weight loss. "
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    ABSTRACT: The incidence of Hodgkin lymphoma (HL) among HIV-infected individuals remains unchanged since the introduction of combination antiretroviral therapy (cART). Recent epidemiological data suggest that CD4 count decline over a year is associated with subsequent diagnosis of HL. In an era of economic austerity monitoring the efficacy of cART by CD4 counts may no longer be required where CD4 count>350 cells/µl and viral load is suppressed (<50 copies/ml). We sought to establish among our HIV outpatient cohort whether a CD4 count decline prior to diagnosis of HL, whether any decline was greater than in patients without the diagnosis, and also whether other clinical or biochemical indices were reliably associated with the diagnosis. Twenty-nine patients with a diagnosis of HL were identified. Among 15 individuals on cART with viral load <50 copies/ml the change in CD4 over 12 months preceding diagnosis of HL was -82 cells/µl (95% CI -163 to -3; p = 0.04). Among 18 matched controls the mean change was +5 cells/µl, 95% CI -70 to 80, p = 0.89). The decline in CD4 over the previous 6-12 months was somewhat greater in cases than controls (mean difference in change -55 cells/µl, 95% CI -151 to 39; p = 0.25). In 26 (90%) patients B symptoms had been present for a median of three months (range one-12) before diagnosis of HL. The CD4 count decline in the 12 months prior to diagnosis of Hodgkin lymphoma among HIV-infected individuals with VL<50 copies/ml on cART was not significantly different from that seen in other fully virologically suppressed individuals in receipt of cART and who did not develop HL. All those who developed HL had B symptoms and/or new palpable lymphadenopathy, suggesting that CD4 count monitoring if performed less frequently, or not at all, among those virologically suppressed individuals with CD4 counts >350 may not have delayed diagnosis.
    PLoS ONE 02/2014; 9(2):e87442. DOI:10.1371/journal.pone.0087442 · 3.23 Impact Factor
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    • "Although HIV-related HL has been strongly linked to the Epstein-Barr virus (EBV), the causes for the increased HL incidence in the cART era remain unclear [14]. Previous studies have described the complex influence of immune function in mediating HL development in this population; however, these studies have been limited by relatively small samples, and findings have been largely inconsistent [10,15-17]. Furthermore, there is limited research examining HIV-related immune factors and immune reconstitution associated with increased HL incidence in a cohort of individuals receiving cART. "
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    ABSTRACT: The incidence of Hodgkin lymphoma (HL) has increased since introduction of combined antiretroviral therapy (cART). While HIV-related HL is highly associated with EBV, the causes underlying the rising incidence remain unclear. The aim of this study was to evaluate the effect of immune reconstitution on HL incidence among a cohort of HIV-infected male veterans ever receiving cART. We performed a retrospective cohort study utilizing data from the Veterans Affairs HIV Clinical Case Registry from 1985-2010. HL cases were identified using ICD-9 codes (201.4-9). Poisson regression was conducted to evaluate relationships between cART-related immunologic measures (e.g., nadir CD4 before cART, time-updated CD4, % time undetectable HIV RNA) and HL incidence. Additionally, we examined CD4 change after cART initiation. 31,056 cART users contributed 287,256 person-years and 196 HL cases (IR=6.8/10,000 person-years). Rate of CD4 increase after cART was worse among HL cases than non-cases (p<0.05). In multivariate regression, HL risk was elevated among veterans with recent CD4 200-350 cells/µL (IRR=1.67, 95%CI=1.16-2.40) and <200 cells/µL (IRR=1.61, 95%CI=1.09-2.39), compared to >350 cells/µL. HL risk was lower among veterans with >80% time undetectable HIV RNA (IRR=0.57, 95%CI=0.35-0.92) and 40-80% undetectable (IRR=0.68, 95%CI=0.47-0.99), compared to <40% undetectable. HL risk was higher in the first 12 months (IRR=2.02, 95%CI=1.32-3.10) and 12-24 months (IRR=1.75, 95%CI=1.16-2.64) after cART initiation, compared to >36 months. These data highlight immunosuppression and poor viral control may increase HL risk, specifically during immune reconstitution in the interval post cART initiation. Findings suggest an immune reconstitution type mechanism in HIV-related HL development.
    PLoS ONE 10/2013; 8(10):e77409. DOI:10.1371/journal.pone.0077409 · 3.23 Impact Factor
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